Worm Breeder's Gazette 14(1): 100 (October 1, 1995)

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.


Shin Murakami, Patricia M. Tedesco, Gordon J. Lithgow, Edward W. Huchinson, Thomas E Johnson

Institute for Behavioral Genetics, University of Colorado, Campus Box 447, Boulder, CO, 80309, USA.

We have been trying to clone age-1 gene.  age-1 was mapped to the left of
unc-4 on chromosome II. The predicted genetic distance between age-1 and
daf-23 is about 2 c.m. Recently, it has been proposed that age-1 and
daf-23 may be allelic, because they do not complement for the Daf-c
phenotype at 27oC (Inoue, T. and Thomas, J., 10th international C.elegans
meeting). To test this possibility, we performed genetical mapping between
age-1 and daf-23 by taking advantage of the Daf-c phenotype. We crossed
TJ1052 [age-1(hx546)] males and daf-23 homozygotes from DR846
{unc-4(e120); daf-23(m333)/mnC1[dpy-10(e128); unc-52(e444)] }(DR846 is
from Don Riddle). The cross produced two F2 recombinants out of  1,261
tested. The genotype of these recombinants indicates that the genetical
distance between age-1 and daf-23 is 0.3 c.m. This result is consistent
with the data that the Daf-c phenotype ofage-1 maps between bli-1 and
rol-1 (Thomas, J., personal communication). This suggests two
      1) age-1 and daf-23 are allelic and 0.3 c.m. reflects intragenic
          recombination, or
      2) age-1 and daf-23 are not allelic but genetically close to each
More precise mapping, such as physical mapping of the two genes, would be
necessary to test these possibilities. Since partial non-complementation
between different genes has been observed in yeast (e.g., Murakami, S.
and Niwa, O., in press), it might be possible that mutations in different
genes fail to complement.

      We have also tried to map age-1 by using chromosome deficiencies
(Dfs). Interestingly, many, but not all, strains carrying deficiencies
around unc-4 or sqt-1 (close to daf-23) produce dauers at 27oC. This
finding suggests that they are haplo-insufficient. Although these Dfs are
not very useful for mapping the Daf-c phenotype of age-1, they may be a
good tool for mapping new Daf-c mutations. A single copy of one or more
genes in these deficiency regions causes dauer formation at this
temperature. We are now mapping these Daf-c responsible regions.
Preliminary results suggest three possible regions: to the left of unc-4,
to the right of unc-4 (this does not include daf-19), and at daf-23.